Rheumatoid arthritis is characterized by systemic inflammation which results in various types of bone loss such as joint erosion and systemic/periarticular osteoporosis. Bone loss occurs based on the imbalance between bone resorption by osteoclasts and bone formation by osteoblasts. The bone loss is mainly caused by enhanced osteoclast formation and activation, which are mediated by RANKL, a key cytokine for osteoclastogenesis. In rheumatoid arthritis, activated T cells accumulate in the synovium where T cells stimulate local inflammation through IL-17, which induce RANKL in synovial cells. This is the main cause of focal bone erosion. Inflammation also influences osteoclastic bone resorption by other mediators such as inflammatory cytokines and IgG immune complex in the serum. They are more related to systemic/periarticular osteoporosis. Less is known about the effect of inflammation on other bone cells, but TNF is known to inhibit bone formation by suppressing Wnt signaling via induction of Dkk-1. Here I summarize the effect of systemic inflammation on bone cells in the context of osteoimmunology.
Disclosure of Interest None declared
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